Salt intake and preference are of particular interest because high salt intake has been implicated in the etiology of hypertension. Salt appetite is a behavioral response to a sodium deficit and is expressed as avid consumption of hypertonic NACl solutions. Salt appetite is subject to sensitization, namely episodes of sodium depletion lead to increased salt appetite following subsequent depletions. Additionally, episodes of acute sodium depletion, in rats, cause an alteration in neuronal morphology with increased dendritic branches and spines in neurons in the nucleus accumbens. Strikingly, these neuronal alterations are remarkably similar to those observed in association with the sensitization to certain addictive drugs. The proposed studies will examine the relationship between sensitization of sodium appetite by prior sodium depletions and altered dendritic morphology in the nucleus accumbens and will assess the relationship of these changes to those associated with drug sensitization. Behavioral and physiological manipulations will involve administration of the natriuretic/diuretic agent, furosemide to produce sodium depletion and promote a sodium appetite. Morphology of neurons in the nucleus accumbens will be analyzed in Golgi stained material and include assessment of total dendritic length, branch length and number as well as spine number and density. The long range goal is to examine the hypothesis that neuronal alterations common to salt and drug sensitization represent a general neuronal response to a strong physiological challenge that provides a mechanism for an enhanced behavioral response to subsequent exposures to that challenge.